Evidence map›Paper›PMID 27475226›Full record

ArticleCell reports2016

Exon Junction Complexes Show a Distributional Bias toward Alternatively Spliced mRNAs and against mRNAs Coding for Ribosomal Proteins.

Christian Hauer, Jana Sieber, Thomas Schwarzl, Ina Hollerer, Tomaz Curk, Anne-Marie Alleaume, Matthias W Hentze, Andreas E Kulozik

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
5.6field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

51 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
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  3. Gene regulation through exon junction complex modularity.Nature structural & molecular biology · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Christian HauerDepartment of Pediatric Oncology, Hematology, and Immunology, University of Heidelberg, Im Neuenheimer Feld 430, 69120 Heidelberg, Germany; Molecular Medicine Partnership Unit (MMPU), Im Neuenheimer Feld 350, 69120 Heidelberg, Germany; European Molecular Biology Laboratory (EMBL) Heidelberg, Meyerhofstrasse 1, 69117 Heidelberg, Germany.
Jana SieberDepartment of Pediatric Oncology, Hematology, and Immunology, University of Heidelberg, Im Neuenheimer Feld 430, 69120 Heidelberg, Germany; Molecular Medicine Partnership Unit (MMPU), Im Neuenheimer Feld 350, 69120 Heidelberg, Germany.
Thomas SchwarzlEuropean Molecular Biology Laboratory (EMBL) Heidelberg, Meyerhofstrasse 1, 69117 Heidelberg, Germany.
Ina HollererDepartment of Pediatric Oncology, Hematology, and Immunology, University of Heidelberg, Im Neuenheimer Feld 430, 69120 Heidelberg, Germany; Molecular Medicine Partnership Unit (MMPU), Im Neuenheimer Feld 350, 69120 Heidelberg, Germany; European Molecular Biology Laboratory (EMBL) Heidelberg, Meyerhofstrasse 1, 69117 Heidelberg, Germany.
Tomaz CurkEuropean Molecular Biology Laboratory (EMBL) Heidelberg, Meyerhofstrasse 1, 69117 Heidelberg, Germany; Faculty of Computer and Information Science, University of Ljubljana, Vecna Pot 113, 1000 Ljubljana, Slovenia.
Anne-Marie AlleaumeEuropean Molecular Biology Laboratory (EMBL) Heidelberg, Meyerhofstrasse 1, 69117 Heidelberg, Germany.
Matthias W HentzeMolecular Medicine Partnership Unit (MMPU), Im Neuenheimer Feld 350, 69120 Heidelberg, Germany; European Molecular Biology Laboratory (EMBL) Heidelberg, Meyerhofstrasse 1, 69117 Heidelberg, Germany. Electronic address: hentze@embl.de.
Andreas E KulozikDepartment of Pediatric Oncology, Hematology, and Immunology, University of Heidelberg, Im Neuenheimer Feld 430, 69120 Heidelberg, Germany; Molecular Medicine Partnership Unit (MMPU), Im Neuenheimer Feld 350, 69120 Heidelberg, Germany. Electronic address: andreas.kulozik@med.uni-heidelberg.de.
European Molecular Biology Laboratory · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The exon junction complex (EJC) connects spliced mRNAs to posttranscriptional processes including RNA localization, transport, and regulated degradation. Here, we provide a comprehensive analysis of bona fide EJC binding sites across the transcriptome including all four RNA binding EJC components eIF4A3, BTZ, UPF3B, and RNPS1. Integration of these data sets permits definition of high-confidence EJC deposition sites as well as assessment of whether EJC heterogeneity drives alternative nonsense-mediated mRNA decay pathways. Notably, BTZ (MLN51 or CASC3) emerges as the EJC subunit that is almost exclusively bound to sites 20-24 nucleotides upstream of exon-exon junctions, hence defining EJC positions. By contrast, eIF4A3, UPF3B, and RNPS1 display additional RNA binding sites suggesting accompanying non-EJC functions. Finally, our data show that EJCs are largely distributed across spliced RNAs in an orthodox fashion, with two notable exceptions: an EJC deposition bias in favor of alternatively spliced transcripts and against the mRNAs that encode ribosomal proteins.

Indexed as

Alternative SplicingCell MembraneExonsHumansRibonucleoproteinsRibosomal ProteinsRNA-Binding ProteinsRNA, MessengerRNA PrecursorsRibonucleoproteinsRibosomal ProteinsRNA-Binding ProteinsRNA, MessengerRNA Precursors

Identifiers

PMID27475226
PMCPMC4978704
OpenAlexW2480770645

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.